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PubMed2024

Environmental epigenetics: Exploring phenotypic plasticity and transgenerational adaptation in fish.

Epigenetics plays a vital role in the interaction between living organisms and their environment by regulating biological functions and phenotypic plasticity. Considering that most aquaculture activities take place in open or natural habitats that are vulnerable to environmental changes. Promising findings from recent research conducted on various aquaculture species have provided preliminary evidence suggesting a link between epigenetic mechanisms and economically valuable characteristics. Environmental stressors, including climate changes (thermal stress, hypoxia, and water salinity), anthropogenic impacts such as (pesticides, crude oil pollution, nutritional impacts, and heavy metal) and abiotic factors (infectious diseases), can directly trigger epigenetic modifications in fish. While experiments have confirmed that many epigenetic alterations caused by environmental factors have plastic responses, some can be permanently integrated into the genome through genetic integration and promoting rapid transgenerational adaptation in fish. These environmental factors might cause irregular DNA methylation patterns in genes related to many biological events leading to organs dysfunction by inducing alterations in genes related to oxidative stress or apoptosis. Moreover, these environmental issues alter DNA/histone methylation leading to decreased reproductive competence. This review emphasizes the importance of understanding the effects of environmentally relevant issues on the epigenetic regulation of phenotypic variations in fish. The goal is to expand our knowledge of how epigenetics can either facilitate or hinder species' adaptation to these adverse conditions. Furthermore, this review outlines the areas that warrant further investigation in understanding epigenetic reactions to various environmental issues.

Animals↗
PubMed2026

Spatiotemporal single-cell profiling reveals T cell clonal dynamics and phenotypic plasticity in human graft-versus-host disease.

Allogeneic hematopoietic cell transplantation cures hematologic diseases but is limited by acute graft‑versus‑host disease. How human T cell clones drive epithelial injury remains poorly mapped. We studied 31 transplant recipients, integrating longitudinal T cell antigen receptor (TCR) profiling with single-cell RNA sequencing/TCR sequencing and spatial transcriptomics to track T cell clonal dynamics. We developed DecompTCR to resolve temporal dynamics and adapted computational tools to map clone phenotypes and niches in tissue. Our analyses revealed that cyclophosphamide selectively depletes alloreactive clones, although insufficient early expansion leads to incomplete depletion and severe disease. Severe graft‑versus‑host disease is marked by persistent expansion of alloreactive clones, rewiring of homeostatic cell types and diversification of donor-derived CD8+ clonotypes that acquire Hobit (ZNF683)+ tissue‑resident memory T (TRM) cell programs during migration to epithelium. Spatial deconvolution identified CD8+ effector/Hobit+ TRM hubs near intestinal stem‑cell-rich crypt bases and crypt‑loss regions. This clonotype‑resolved framework links tissue‑instructed TRM cell remodeling to localized epithelial injury, nominating early-repertoire dynamics and spatial hub burden as biomarkers.

Journal Article↗
PubMed2026

Coral color morphs exhibit distinct microbial and proteomic profiles linked to stress and immune mechanisms in a changing ocean.

BACKGROUND: Coral phenotypic plasticity facilitates acclimation and adaptation to environmental variability. Coral species often display a variety of color morphs, yet key biological and ecological implications of such phenotypic variation remain underexplored. Here, we present the first proteomic and untargeted lipidomic and metabolomic survey to explore the biological characteristics and potential ecological significance of different color morphs (pink and brown) of healthy Pocillopora verrucosa sampled along a latitudinal gradient. RESULTS: Our multi-omic approach elucidated distinct mechanisms associated with these dominant color morphs. We discovered bacterial indicators specific to each morph: putative pathogens such as Salmonella, Escherichia-Shigella, and carotenoid-producing Gemmatimonas were notably associated with the pink morph, whereas the brown morph was associated with potentially beneficial bacteria, such as Lysobacter, Acinetobacter, and Endozoicomonas. Despite these microbiome differences, the lipidome and metabolome of P. verrucosa were surprisingly homogeneous across colors and locations, suggesting similar metabolic performances during summer conditions. Key polar and apolar lipid classes, such as fatty acids, glycerophosphocholines, and retinoids, were prevalent. Notably, our proteomic analysis revealed morph-specific expressions, with pink morphs exhibiting enhanced levels of GFP-like proteins, Ankyrin, and the enzyme pullulanase, suggesting novel putative protective roles. In contrast, the brown morphs showed a higher abundance of heat shock proteins, indicating putative differential stress response capabilities. CONCLUSION: This comprehensive study provides the first proteomic survey of P. verrucosa and identifies key physiological pathways and trade-offs linked to color morphs, which can further contribute to enhancing our understanding of coral resilience in the face of climate change. SIGNIFICANCE STATEMENT: Understanding the phenotypic plasticity of corals is crucial for uncovering mechanisms of resilience in warming oceans, yet the biological significance of coral color morphs still needs to be explored. Using an innovative multi-omic approach (proteomics, lipidomics, and metabolomics), we provide the first comprehensive analysis of differences between pink and brown morphs of Pocillopora verrucosa. Our data reveal key taxa, potentially pathogenic or beneficial, associated with each morph, and suggest different strategies for each color morph to cope with heat stress, either expressing proteins involved in UV protection and heterotrophic activity or enhanced levels of heat stress resilience and DNA repair. These findings offer insights into the phenotypic plasticity of coral color morphs and their differential responses to climate change. Video Abstract.

Anthozoa↗
PubMed2026

The Multiple Roles of Genetics on Freshwater Macrophyte Functional Traits in the Interplay With the Environment: A Review.

The study of functional trait variation is increasingly used to understand macrophyte adaptation, as traits reflect organismal performance under different ecosystem conditions. Phenotypic expression results from the interplay of genetic and environmental factors: genetics provides the molecular basis for heritable traits and constrains potential phenotypes, while the environment acts as a selective and modulatory force. However, the genetic insight into traits has rarely been addressed in freshwater macrophyte studies. This review examines the different ways in which the DNA of macrophytes interplays with the environment and contributes to the variation in their functional traits, outlining main approaches, gaps, and future challenges. Only 21 studies explicitly combined genetics with functional traits and environment in the last fifteen years. The most common approach was the use of common garden experiments to explore acclimation and adaptation in a few model species. Current studies mainly focus on morphological and growth traits that best describe macrophytes' economic strategies, with limited attention to other trait categories, while the genetic and DNA traits studied are more variable. Across studies, environmental factors generally explained a larger proportion of functional trait variation, highlighting the dominant role of phenotypic plasticity for macrophyte acclimatation, whereas genetic contribution increased under experimentally manipulated conditions. Genome size and epigenetic variation influenced phenotypic plasticity; however, the effect was different and inconsistent on traits and depended on phylogenetic relationships and geographical environment variation. In field studies of natural populations, life history traits and hydrology had a strong effect on the geographic distribution of genetic diversity and the response to selection, as well as on our ability to distinguish selection from genetic drift. Future research should enhance molecular analyses, adopt multifactorial and long-term experimental designs, develop conceptual frameworks to address the relationships between genomics, environment and functional traits and integrate emerging tools to capture macrophyte adaptation better.

adaptation↗
PubMed2026

Maternal and developmental temperature modulate adult response to temperature in Drosophila melanogaster.

Beyond inherited genes and environmentally induced changes in gene expression, phenotypes can also be shaped by parental effects-an effect from a parental phenotype that causes modifications in offspring traits, which cannot be solely explained by the parental or offspring genomes. Such effects may prepare offspring for future environmental conditions and contribute to phenotypic plasticity, including responses to temperature. While temperature-induced plasticity has been extensively studied, the relative contributions of parental versus direct environmental cues remain poorly understood. The fruit fly Drosophila melanogaster is a powerful model for studying physiological and behavioral adaptation to temperature. Flies inhabit environments spanning broad thermal ranges and show evidence of parental effects, such as increased heat tolerance in offspring from warm-reared parents. Here, we exposed mothers to two experimental temperatures and split their broods between the same two temperatures to estimate the relative importance of maternal and developmental effects on adult physiological and developmental responses to temperature. We find that the reaction norms of locomotor activity under gradually increasing temperatures, responses to heat-shock and cold-shock, and fecundity are mostly governed by direct plastic responses to developmental environment. We detected comparatively weak maternal effects in the response to heat-shock, fecundity, and grand-offspring survival where matched environments counteracted the effects of direct offspring experience. We conclude that thermal experience during development is the primary determinant of phenotypic plasticity in D. melanogaster, while maternal experience contributes a small but non-negligible component.

Animals↗
PubMed2025

Whole Genome Sequencing Reveals How Plasticity and Genetic Differentiation Underlie Sympatric Morphs of Arctic Charr.

Salmonids have a remarkable ability to form sympatric morphs after postglacial colonisation of freshwater lakes. These morphs often differ in morphology, feeding and spawning behaviour. Here, we explored the genetic basis of morph differentiation in Arctic charr (n = 283) by first establishing a high-quality reference genome and then using this in whole genome sequencing of distinct morphs present in two Norwegian and two Icelandic lakes. The four lakes represent the spectrum of genetic differentiation between morphs from one lake with no genetic differentiation between morphs, implying phenotypic plasticity, to two lakes with locus-specific genetic differentiation, implying incomplete reproductive isolation, and one lake with strong genome-wide divergence consistent with complete reproductive isolation. As many as 12 putative inversions ranging from 0.45 to 3.25 Mbp in size segregated among the four morphs present in one lake, Thingvallavatn, and these contributed significantly to the genetic differentiation among morphs. None of the putative inversions were found in any of the other lakes, but there were cases of partial haplotype sharing in similar morph contrasts in other lakes. Our findings are consistent with a highly polygenic basis of morph differentiation with population-specific selection on alleles linked to the development of similar morph phenotypes. The results support a model where morph differentiation is first established through phenotypic plasticity, leading to niche expansion and separation. This may be followed by gradual development of reproductive isolation, locus-specific differentiation and eventually complete reproductive isolation and genome-wide divergence.

Whole Genome Sequencing↗
PubMed2025

Silent cells? Potential for context-dependent gene expression in mature sperm.

Sperm are traditionally viewed as transcriptionally and translationally silent cells. However, observations that components of the cellular machinery of gene expression are maintained in ejaculated sperm are increasingly cited as challenges to this fundamental assumption. Here, we critically evaluate these arguments and present three lines of evidence from both model and non-model systems that collectively raise the question of whether ejaculated sperm may be capable of active gene expression. First, and critical for arguments surrounding the possibility of differential gene expression, we review recent evidence that spermatozoa may retain the capacity to transcribe and translate their genomes. Second, we highlight how sperm cells can exhibit differential transcript quantities across different post-ejaculation environments. Third, we ask whether the accumulating evidence of remarkable phenotypic plasticity in post-ejaculatory sperm phenotypes could be mechanistically underpinned by changes in sperm gene expression. While these lines of evidence are indirect and do not definitively show transcription of sperm genomes, we highlight how emerging technologies may enable us to test this hypothesis explicitly. Our review advocates for progress in this field and highlights several important evolutionary, ecological and practical implications that will probably transcend disciplines to the clinical and applied reproductive sectors.

Male↗
PubMed2026

Stress-driven strategic games in cancer.

Tumor cells face chronic genotoxic, metabolic, hypoxic, and immune stress that shapes their evolution. While stress-response molecular pathways are well characterized, cancer biology lacks a predictive framework for how cells select among alternative adaptive strategies and how these selections interact to produce tumor-level behavior. We propose that evolutionary game theory, previously applied to cooperation in cancer, should be extended to position stress adaptation itself as the organizing principle of tumor evolution. In this framework, stress-adaptive strategies constitute frequency-dependent games whose payoffs depend on population composition. We introduce a three-level distinction between cell states (transcriptional snapshots), game states (local configurations of stress and neighbor composition that define the active payoff structure), and cell strategies (conditional behavioral policies mapping game states to fitness-relevant outputs). This perspective explains the maintenance of intratumor heterogeneity through frequency-dependent selection, the reversibility of resistance through bet-hedging dynamics, and therapy resistance as an equilibrium outcome rather than genetic inevitability. Integrating insights from single-cell genomics, spatial profiling, and lineage tracing, we outline testable predictions and experimental approaches for measuring payoff structures. Therapeutically, the framework suggests exploiting adaptive trade-offs, restricting phenotypic plasticity, and reshaping competitive landscapes. Re-framing cancer as an evolving game of stress adaptation provides a unifying structure for predictive oncology.

Animals↗
PubMed2026

Adaptations to breath-hold diving: from traditional divers to elite athletes.

Breath-hold diving exposes humans to repeated episodes of profound hypoxia and hypercapnia, eliciting physiological adaptations that enable prolonged underwater performance. This article summarises current knowledge on chronic adaptations in elite breath-hold athletes and traditional diving populations, including the Bajau sea nomads of Southeast Asia and the Korean Haenyeo divers. Evidence indicates that repeated apnoea induces adaptations across multiple physiological systems. Haematological changes include increased spleen size and enhanced splenic contraction, augmenting circulating haemoglobin and oxygen stores during apnoea. In elite divers, structured training can increase resting spleen volume, whereas the Bajau exhibit genetically associated splenic enlargement linked to variants near the PDE10A gene. Cardiopulmonary adaptations include modified pulmonary vascular responses to hypoxia, improved oxygen conservation, and metabolic shifts favoring efficient mitochondrial energy production. Molecular adaptations involve enhanced antioxidant defenses and activation of hypoxia-responsive pathways that may mitigate oxidative stress associated with repeated hypoxia-reoxygenation cycles. Emerging evidence also suggests neural plasticity and possible structural brain adaptations, although the long-term neurological consequences of chronic intermittent hypoxia exposure remain uncertain. Studies of traditional diving populations indicate that both phenotypic plasticity and genetic selection contribute to diving capacity, highlighting interactions between training and evolution. Despite these benefits, breath-hold diving also carries risks, including hypoxic blackout, decompression sickness, and potential neurological injury. Understanding the mechanisms underlying human tolerance to extreme hypoxia may have implications beyond diving physiology, including applications in cardiovascular medicine, hypoxic diseases, and rehabilitation. Further longitudinal, genomic, and mechanistic studies are needed to clarify the limits, benefits, and clinical relevance of these adaptations.

Humans↗
PubMed2024

A Proteogenomic Pipeline for the Analysis of Protein Biosynthesis Errors in the Human Pathogen Candida albicans.

Candida albicans is a diploid pathogen known for its ability to live as a commensal fungus in healthy individuals but causing both superficial infections and disseminated candidiasis in immunocompromised patients where it is associated with high morbidity and mortality. Its success in colonizing the human host is attributed to a wide range of virulence traits that modulate interactions between the host and the pathogen, such as optimal growth rate at 37 °C, the ability to switch between yeast and hyphal forms, and a remarkable genomic and phenotypic plasticity. A fascinating aspect of its biology is a prominent heterogeneous proteome that arises from frequent genomic rearrangements, high allelic variation, and high levels of amino acid misincorporations in proteins. This leads to increased morphological and physiological phenotypic diversity of high adaptive potential, but the scope of such protein mistranslation is poorly understood due to technical difficulties in detecting and quantifying amino acid misincorporation events in complex protein samples. We have developed and optimized mass spectrometry and bioinformatics pipelines capable of identifying rare amino acid misincorporation events at the proteome level. We have also analyzed the proteomic profile of an engineered C. albicans strain that exhibits high level of leucine misincorporation at protein CUG sites and employed an in vivo quantitative gain-of-function fluorescence reporter system to validate our LC-MS/MS data. C. albicans misincorporates amino acids above the background level at protein sites of diverse codons, particularly at CUG, confirming our previous data on the quantification of leucine incorporation at single CUG sites of recombinant reporter proteins, but increasing misincorporation of Leucine at these sites does not alter the translational fidelity of the other codons. These findings indicate that the C. albicans statistical proteome exceeds prior estimates, suggesting that its highly plastic phenome may also be modulated by environmental factors due to translational ambiguity.

Candida albicans↗
PubMed2025

Machine learning on multiple epigenetic features reveals H3K27Ac as a driver of gene expression prediction across patients with glioblastoma.

Epigenetic mechanisms play a crucial role in driving transcript expression and shaping the phenotypic plasticity of glioblastoma stem cells (GSCs), contributing to tumor heterogeneity and therapeutic resistance. These mechanisms dynamically regulate the expression of key oncogenic and stemness-associated genes, enabling GSCs to adapt to environmental cues and evade targeted therapies. Importantly, epigenetic reprogramming allows GSCs to transition between cellular states, including therapy-resistant mesenchymal-like phenotypes, underscoring the need for epigenetic-targeting strategies to disrupt these adaptive processes. Understanding these epigenetic drivers of gene expression provides a foundation for novel therapeutic interventions aimed at eradicating GSCs and improving glioblastoma outcomes. Using machine learning (ML), we employ cross-patient prediction of transcript expression in GSCs by combining epigenetic features from various sources, including ATAC-seq, CTCF ChIP-seq, RNAPII ChIP-seq, H3K27Ac ChIP-seq, and RNA-seq. We investigate different ML and deep learning (DL) models for this task and ultimately build our final pipeline using XGBoost. The model trained on one patient generalizes to other 11 patients with high performance. Notably, H3K27Ac alone from a single patient is sufficient to predict gene expression in all 11 patients. Furthermore, the distribution of H3K27Ac peaks across the genomes of all patients is remarkably similar. These findings suggest that GSCs share a common distributional pattern of enhancer activity characterized by H3K27Ac, which can be utilized to predict gene expression in GSCs across patients. In summary, while GSCs are known for their transcriptomic and phenotypic heterogeneity, we propose that they share a common epigenetic pattern of enhancer activation that defines their underlying transcriptomic expression pattern. This pattern can predict gene expression across patient samples, providing valuable insights into the biology of GSCs.

Glioblastoma↗
PubMed2025

Multiomics Reveal Associations Between CpG Methylation, Histone Modifications and Transcription in a Species That has Lost DNMT3, the Colorado Potato Beetle.

Insects display exceptional phenotypic plasticity, which can be mediated by epigenetic modifications, including CpG methylation and histone modifications. In vertebrates, both are interlinked and CpG methylation is associated with gene repression. However, little is known about these regulatory systems in invertebrates, where CpG methylation is mainly restricted to gene bodies of transcriptionally active genes. A widely conserved mechanism involves the co-transcriptional deposition of H3K36 trimethylation and the targeted methylation of unmethylated CpGs by the de novo DNA methyltransferase DNMT3. However, DNMT3 has been lost multiple times in invertebrate lineages raising the question of how the links between CpG methylation, histone modifications and gene expression are affected by its loss. Here, we report the epigenetic landscape of Leptinotarsa decemlineata, a beetle species that has lost DNMT3 but retained CpG methylation. We combine RNA-seq, enzymatic methyl-seq and CUT&Tag to study gene expression, CpG methylation and patterns of H3K36me3 and H3K27ac histone modifications on a genome-wide scale. Despite the loss of DNMT3, H3K36me3 mirrors CpG methylation patterns. Together, they give rise to signature profiles for expressed and not expressed genes. H3K27ac patterns show a prominent peak at the transcription start site that is predictive of expressed genes irrespective of their methylation status. Our study provides new insights into the evolutionary flexibility of epigenetic modification systems that urge caution when generalizing across species.

Animals↗
PubMed2026

Overcoming cancer resistance in pancreatic cancer: toward dynamic precision oncology.

Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal malignancy, largely because of its profound and evolving therapeutic resistance. Resistance is not determined by a single molecular alteration but arises from interconnected mechanisms, including intrinsic resistance, treatment-induced adaptive resistance, acquired resistance, genomic evolution, clonal selection, cancer stemness, phenotypic plasticity, metabolic adaptation, and tumor microenvironment-mediated effects. Emerging therapeutic approaches targeting KRAS/RAS signaling, stromal and immune components, metabolic dependencies, and DNA damage repair pathways offer opportunities to address these mechanisms, although durable efficacy remains limited by biological heterogeneity and adaptive responses. In this review, we examine therapeutic resistance as an evolutionary and multidimensional process and summarize emerging strategies for overcoming resistance. We further propose a Dynamic Precision Oncology (DPO) framework that extends conventional precision oncology beyond baseline molecular profiling by integrating longitudinal assessment of tumor genomics, circulating tumor DNA, CA19-9, imaging, radiomics, and clinical characteristics. This framework emphasizes iterative detection and characterization of emerging resistance, mechanism-informed treatment adaptation, and subsequent reassessment rather than automatic treatment modification based on a single biomarker. DPO may provide a conceptual framework for integrating evolving tumor biology into treatment decision-making, while prospective studies are needed to validate biomarkers, define actionable thresholds, and determine whether longitudinal resistance-guided strategies improve clinical outcomes in PDAC.

Humans↗
PubMed2026

The Brazilian contribution to ant toxinology: challenges and perspectives.

Ant toxinology in Brazil is a small but growing field that has revealed wide biochemical diversity and clear potential for bioprospecting therapeutic molecules. This review compiles the Brazilian contribution, focusing on advances in the characterization of venoms from medically and ecologically important species of Dinoponera, Solenopsis, Paraponera, Pachycondyla, Neoponera, and Ectatomma. Brazilian groups applied omics approaches, including transcriptomics and proteomics, to resolve the composition of these venoms and identified peptide-rich arsenals with antimicrobial, antiparasitic, antitumor, and neuroactive activity. Studies of venom phenotypic plasticity showed ecological factors such as diet and seasonality shape venom composition. Two challenges persist: assigning function to still unidentified components and obtaining venom in the quantities that broad analysis requires. The near-term prospects are the rational design of peptide analogues with improved activity and continued bioprospecting of new species, which together position Brazil as a central contributor to ant toxinology.

Animals↗
PubMed2026

Genome-wide SNP data support species boundaries in sympatric Polylepis Ruiz & Pav. (Rosaceae) species from Bolivia and Ecuador.

Species delimitation in the South American genus Polylepis is notoriously challenging due to high morphological similarity and phenotypic plasticity, likely driven by hybridization and gene flow. Previous phylogenetic studies suggested that genetic structure aligns more strongly with geography than with taxonomy, questioning existing species concepts and hampering conservation efforts. We used double-digest RAD sequencing (ddRADseq) to generate genome-wide SNP data for 11 Polylepis species sampled across multiple localities in Bolivia and Ecuador. Population genetic analyses, phylogenetic inference, and network approaches were combined to assess whether genetic structure aligns more closely with taxonomy or geography. Morphologically defined species formed largely cohesive genetic lineages across regions, with species identity explaining substantially more genetic variation than locality. While localized admixture and reticulation were detected among closely related taxa, widespread species showed strong genetic cohesion and clear separation from congeners. Our results indicate that the sampled Polylepis species from Bolivia and Ecuador maintain distinct genetic identities despite localized signals consistent with gene flow. This genome-wide support for current taxonomy highlights Polylepis as a valuable model for studying speciation under gene flow and indicates that multiple geographic sampling will be essential in reconstructing a robust phylogeny of the genus, with important implications for conservation planning in Andean montane forests.

Bolivia↗
PubMed2026

A single-cell lens into the co-evolution of genotypes and phenotypes in cancer.

Genetic heterogeneity and clonal outgrowths are observed even in otherwise healthy human tissues, shaping the genetic composition of cell populations in non-malignant disease and during physiological ageing. This clonal mosaicism likely provides the pre-cancerous seeds for malignant transformation. Once a tumour arises, clonal evolution poses a major challenge to achieving cure, as clonal diversification provides an expanded number of substrates upon which therapy can act as a selective pressure, leading to the selection of resistant clones that ultimately fuel disease recurrence. Understanding somatic clonal evolution requires not only mapping genetic diversity but also defining the resulting phenotypes that provide a fitness advantage to mutated clones. This Review discusses multimodal single-cell technologies that enable the measurement of genotypes and additional molecular features from the same cell. These technologies unveil mutant-specific phenotypic traits, often show cell-state specificity in genotype-phenotype effects and can define therapeutic vulnerabilities for precision elimination of disease-propagating mutant cells. Furthermore, the combination of phylogenetic reconstruction with phenotypic measurements allows for the temporal mapping of clonal evolution and phenotypic plasticity. These breakthroughs have created a unique opportunity to define, directly in primary human samples, the mechanisms underlying clonal expansion in both healthy and malignant tissues.

Journal Article↗
PubMed2026

Adaptive evolution of polyploid crops.

Crop evolution represents a fundamental biological process through which plants respond to selection in different environments. This encompasses mechanisms operating at multiple scales of biological organization, including genetic and epigenetic regulation and higher-order interactions among molecular complexes. This Review synthesizes how polyploidy shapes crop evolution by generating duplicated genes, driving genome reorganization, altering dosage relationships and promoting regulatory divergence, which together influence crop metabolism, physiology, development and environmental responses. We focus mainly on the mechanisms underlying adaptation in polyploid crops, including the consequences of gene and genome duplication, genome reorganization and subfunctionalization. We also examine how hybridization, phenotypic plasticity and crop-microbiome interactions intersect with polyploidy to expand or constrain adaptive potential. Together, these processes affect crop survival, fitness and breeding value under changing environments. We suggest that future research connect polyploid genome architecture with experimentally validated signatures of selection and field performance to make better use of polyploidy-derived variation in crop improvement.

Polyploidy↗
PubMed2026

ChromCall: assigning chromatin status to defined genomic regions using epigenomic profiling data.

MOTIVATION: Chromatin regulation is crucial for modulating gene expression and cellular function by altering DNA accessibility. Defining and understanding chromatin regulation across diverse biological conditions, including health and disease, requires quantification of both the presence and enrichment level of diverse DNA-binding factors and chromatin modifications across defined genomic regions. Existing approaches mainly rely on peak-based or genome-wide models, which identify high-signal regions but do not annotate chromatin status at predefined functional genomic regions, such as promoters or enhancers. This lack of region-based annotation limits downstream comparative and integrative analyses across multiple factors and datasets, prompting us to create ChromCall. RESULTS: ChromCall is an R package for region-based chromatin enrichment analysis that provides a robust and extensible foundation for transparent and reproducible epigenomic profiling at predefined genomic regions. We applied ChromCall to ChIP-seq data from glioblastoma (GBM) brain tumours and found that the promoters of genes implicated in treatment resistance are significantly more likely to exhibit a combination of histone marks associated with phenotypic plasticity. This highlights a potential novel mechanism of therapeutic escape in these deadly tumours. AVAILABILITY AND IMPLEMENTATION: The R package is available on https://github.com/GliomaGenomics/ChromCall and the version used in this paper is archived at https://doi.org/10.5281/zenodo.19580967.

Chromatin↗